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Relationship of neurofibrillary pathology to cerebral amyloid angiopathy in Alzheimer's disease
Author(s) -
Williams S.,
Chalmers K.,
Wilcock G. K.,
Love S.
Publication year - 2005
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.2005.00663.x
Subject(s) - cerebral amyloid angiopathy , pathology , cortex (anatomy) , senile plaques , alzheimer's disease , amyloid (mycology) , cerebral cortex , apolipoprotein e , cerebral arteries , amyloid beta , temporal cortex , angiopathy , parenchyma , medicine , anatomy , biology , neuroscience , dementia , disease , endocrinology , diabetes mellitus
Over 90% of patients with Alzheimer's disease (AD) develop cerebral amyloid angiopathy (CAA). Severe dyshoric CAA, in which amyloid extends into the surrounding brain parenchyma, may be associated with adjacent clustering of tau‐immunopositive neurites but the relationship of CAA to neurofibrillary pathology has not been systematically investigated. In the present study this relationship was examined in sections of frontal, temporal and parietal cortex from 25 AD patients with moderate to severe CAA and 26 with mild or absent CAA. We measured immunolabelling of abnormally phosphorylated tau adjacent to Aβ‐laden and non‐Aβ‐laden arteries and arterioles, and in cortex away from arteries and arterioles. We also analysed the possible influence of APOE genotype on these measurements. There were no significant differences between the lobes in measurements of tau labelling, either around blood vessels or elsewhere in the cortex. However, tau labelling around Aβ‐laden arteries and arterioles significantly exceeded that around non‐Aβ‐laden blood vessels ( P < 0.001) and this, in turn was greater than the labelling of cortex away from blood vessels ( P < 0.001). There was no association between APOE ɛ4 and the immunolabelling density for tau, whether around amyloid‐ or non‐amyloid‐laden arteries and arterioles, or in the cerebral cortex away from these. We propose that both CAA and peri‐vascular accumulation of hyperphosphorylated tau may be a consequence of elevated levels of soluble Aβ around cortical arteries and arterioles.